Key result
Distinct platelet transcriptomic signatures in women with MI link to future MACE.
Why the study?
Although platelets play a critical pathogenic role in MI, few studies have characterized the MI platelet transcriptome in the acute or chronic setting in women.
Does the platelet transcriptome differ between women with myocardial infarction and controls, and between MI subtypes?
Observational (n=78)
Yes
Does the platelet transcriptome differ between women with myocardial infarction and controls, and between MI subtypes?
Platelets from women with myocardial infarction exhibit a distinct transcriptomic signature that differentiates MI subtypes and remains stable over time, containing genes that predict long-term adverse cardiovascular outcomes.
Answers are grounded in this paper and cite their sources.
May inform post-MI risk stratification in women via platelet transcripts; hypothesis-generating and requires prospective validation before clinical adoption.
Although platelets play a critical pathogenic role in myocardial infarction (MI), few studies have characterized the MI platelet transcriptome in the acute or chronic setting in women. We report that transcripts associated with the actin cytoskeleton, Rho family GTPases, mitochondrial dysfunction, and inflammatory signaling are enriched in platelets from MI patients in the acute setting (n = 40, MI; n = 38, control) and do not significantly change over time. Furthermore, 79 platelet genes chronically elevated or suppressed after MI are associated with future cardiovascular events in an independent high-risk cohort (n = 135). Compared with women with MI with nonobstructive coronary arteries, platelets from women with MI and obstructive coronary artery disease were enriched in neutrophil activation and proinflammatory signaling pathways driven by increased tumor necrosis factor (TNF)-α signaling. Hierarchic clustering of the MI transcriptomic profile identified 3 subgroups with distinctive biological pathways and MI correlates. Our data demonstrate that platelets from MI patients are phenotypically different from MI-naïve patients in the acute and chronic settings and reveal a platelet transcriptomic signature with distinct clinical features.
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Barrett et al. (2024) conducted an observational in Myocardial Infarction in Women (n=78). Myocardial Infarction vs. Stable cardiac symptoms without MI (Control) was evaluated on Differentially expressed platelet transcripts in MI vs control (p=<0.05). Women with myocardial infarction exhibited 1,421 differentially expressed platelet genes compared to controls, with enriched inflammatory and cytoskeletal pathways, 59 of which independently predicted future major adverse cardiac events.
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